I am a former EUROCONTROL software analyst-programmer in Flight Plan Processing at Karlsruhe UIR control center Karlsruhe with operational responsibility of maintenance and enhancement 1992 - 1997. My experience is in large systems also outside the ATC area. Systems psychology and human computer interaction areas are of special interest to me and I have taught in these areas at Istanbul Yeditepe University computer department.

Working on Large Systems is a
serious commitment which may end up with various disasters.I will mention only three of the mental risks
that may cause burn-out in the simplest possibilities or serious psychotic
problems.

“Under acute
stress—think “fight or flight”—the hypothalamus churns out corticotropin-releasing
hormone, prompting a sharp rise in the stress hormone cortisol, which enhances
immunity, memory, energy and cardiovascular function. Once the stressor has
passed, the hormone DHEA, neuropeptide Y and other biochemicals rush in,
restoring equilibrium and easing symptoms, such as hypertension. Acutely, these
mediators, along with emotional engagement with a task, may enhance learning.

“Chronic over-secretion of stress
hormones adversely affects brain function, especially memory. Too much cortisol
can prevent the brain from laying down a new memory, or from accessing already
existing memories.[2]”

“The renowned brain researcher, Robert M. Sapolsky, has shown that
sustained stress can damage the hippocampus , the part of the limbic brain
which is central to learning and memory. The culprits are "glucocorticoids,"
a class of steroid hormones secreted from the adrenal glands during stress.
They are more commonly know as corticosteroids or cortisol.[2]”

“Excessive cortisol can make it difficult to think or retrieve long-term
memories. That's why people get befuddled and confused in a severe crisis.
Their mind goes blank because "the lines are down." They can't
remember where the fire exit is, for example.[2]”

Norepinephrine balances the bad sideeffects of cortisol.A highly motivated person working under heavy
load goes into a potential disaster if something happens that removes the
motivation abruptly.Norepinephrine
supply suddenly stops and his brain faces an abundant amount of cortisol
alone.This is why motivation control
both by individuals and the management is so important on large systems.A manager can easily and permanently hurt an
employee who is working under heavy load with high motivation.Punish the person who expects a reward.He will be mentally sacked.

2-Kindling
namely growth of neural paths unconsciously under continuous stress.This may explain the situations when somebody
feels stress without any reason or remembers a stressful experience at the
moment he feels stress about an important problem triggered by some other and
simple reason.

"Kindling rewires the brain. … the
brain reshapes itself anatomically in response to small noxious stimuli. …
Kindling appears to be a kind of learning, but a learning that can occur
independent of cognition. … Illness, once expressed, can become responsive to
ever smaller stimuli and, in time, independent of stimuli altogether. The
expression of the disorder becomes more complex over time[3]."

“Over
time, repeated stressful experiences can literally, not just figuratively,
alter the nervous systems of the temperamentally vulnerable. Animal research
has shown that when a rat is given a small shock, it shows no marked reaction;
when exposed to such stressors for five consecutive days, it shows signs of the
stress response; when exposed for seven or eight days, the rat has a seizure,
and thereafter this 'kindled' animal will seize with little or no provocation[3].

When a
temperamentally vulnerable person is constantly bombarded with upsetting
stimuli, Gold says, the genes that get turned on are those involved in the
cellular components of the stress response[3]."

"Suppose a major traumatic
stressor occurs, of a sufficient magnitude to disrupt hippocampal function
while enhancing amygdaloid function. At some later point, in a similar setting,
you have an anxious, autonomic state, agitated and fearful, and you haven't a
clue why—this is because you never consolidated memories of the event via your
hippocampus while your amygdala-mediated autonomic pathways sure as hell
remember[3]."

People who have few and weakly inadequate social relations are at the risk
of getting smaller amygdala and hence they are faced with the risk of getting
related mental problems:“Postmortem studies
ofschizophrenic patients have found
significant amygdala volume reductions as well as of other medial lymbic
structures (Bogerts 1984; Bogerts et all., 1985)[6]”.

Bruce
McEwen, a professor of neuroendocrinology at the Rockefeller University, The Embattled Brain.

Linking the nervous and endocrine
systems, biochemical mediators regulate the effects of stress, which are
exacerbated by health-related behaviors such as inactivity or poor diet. Under acute
stress—think “fight or flight”—the hypothalamus churns out
corticotropin-releasing hormone, prompting a sharp rise in the stress hormone
cortisol, which enhances immunity, memory, energy and cardiovascular function.
Once the stressor has passed, the hormone DHEA, neuropeptide Y and other
biochemicals rush in, restoring equilibrium and easing symptoms, such as
hypertension. Acutely, these mediators, along with emotional engagement with a
task, may enhance learning.

But when stress is chronic, cortisol erodes health. Immune
suppression, hypertension, bone mineral loss, muscle wasting and metabolic
disorders ensue. Within the hippocampus and amygdala, seats of memory and
emotion, dendrites shrink and synapses vanish, McEwen has shown. Cognitive
function declines, depression sinks in, the immune system weakens, and
metabolism goes awry. In
a study of medical students preparing for board exams, McEwen’s collaborators
found that higher levels of perceived stress predicted poor mental flexibility
and reduced functional connectivity in the prefrontal cortex.

The good news: These ill effects are reversible, McEwen
said. Regular exercise returns the hippocampus to normal size and improves
memory, for example, while mindfulness training reduces the amygdala’s volume
and curbs anxiety. Many
adult diseases could be prevented by reducing toxic stress in utero and in
early childhood, he said.

The ambulance
siren screams it’s warning to get out of the way. You can’t move your car
because you’re stuck in a bumper-to-bumper traffic jam that reaches as far as
the eye can see. There must be an accident up ahead. Meanwhile the road
construction crew a few feet from your car is jack-hammering the pavement. You
are about to enter the stress zone.

Hormones rush to your adrenal glands to suppress
the streaming cortisol on its way to your brain. Other hormones rush to your
brain to round up all the remnants of cortisol missles that made it to your
hippocampus. These hormones escort the cortisol remnants back to Kidneyland for
a one-way ride on the Bladderhorn. You have now reached metabolic equilibrium,
also known as homeostasis.

...

Stress and
Memory

Chronic over-secretion of stress hormones
adversely affects brain function, especially memory. Too much cortisol can
prevent the brain from laying down a new memory, or from accessing already existing
memories.

The renowned brain researcher, Robert M. Sapolsky,
has shown that sustained stress can damage the hippocampus , the part of the
limbic brain which is central to learning and memory. The culprits are
"glucocorticoids," a class of steroid hormones secreted from the
adrenal glands during stress. They are more commonly know as corticosteroids or
cortisol .

During a perceived threat, the adrenal glands
immediately release adrenalin. If the threat is severe or still persists after
a couple of minutes, the adrenals then release cortisol. Once in the brain
cortisol remains much longer than adrenalin, where it continues to affect brain
cells.

Cortisol
Affects Memory Formation and Retrieval

Have you ever
forgotten something during a stressful situation that you should have
remembered? Cortisol also interferes with the function of neurotransmitters,
the chemicals that brain cells use to communicate with each other.

Excessive cortisol can make it difficult to think
or retrieve long-term memories. That's why people get befuddled and confused in
a severe crisis. Their mind goes blank because "the lines are down."
They can't remember where the fire exit is, for example.

Why We Lose Our
Memory

Stress hormones divert blood glucose to exercising
muscles, therefore the amount of glucose – hence energy – that reaches the
brain's hippocampus is diminished. This creates an energy crisis in the
hippocampus which compromises its ability to create new memories.

That may be why
some people can't remember a very traumatic event, and why short-term memory is
usually the first casualty of age-related memory loss resulting from a lifetime
of stress.

Cortisol and
Temporary Memory Loss-Study

In an animal
study, rats were stressed by an electrical shock, and then made to go through a
maze that they were already familiar with. When the shock was given either four
hours before or two minutes before navigating the maze, the rats had no
problem. But, when they were stressed by a shock 30 minutes before, the rats were
unable to remember their way through the maze.

This time-dependent effect on memory performance
correlates with the levels of circulating cortisol, which are highest at 30
minutes. The same thing happened when non-stressed rats were injected with cortisol.
In contrast, when cortisol production was chemically suppressed, then there
were no stress-induced effects on memory retrieval.

According to
James McGaugh, director of the Center for the Neurobiology of Learning and
Memory at the University of California, Irvine, "This
effect only lasts for a couple of hours, so that the impairing effect in this
case is a temporary impairment of retrieval. The memory is not lost. It is just
inaccessible or less accessible for a period of time."12

Cortisol and
the Degenerative Cascade

Normally, in response to stress, the brain's
hypothalamus secretes a hormone that causes the pituitary gland to secrete
another hormone that causes the adrenals to secrete cortisol. When levels of
cortisol rise to a certain level, several areas of the brain – especially the
hippocampus – tell the hypothalamus to turn off the cortisol-producing
mechanism. This is the proper feedback response.

The hippocampus, however, is the area most damaged
by cortisol. In his book Brain Longevity, Dharma Singh Khalsa, M.D., describes
how older people often have lost 20-25% of the cells in their hippocampus, so
it cannot provide proper feedback to the hypothalamus, so cortisol continues to
be secreted. This, in turn, causes more damage to the hippocampus, and even
more cortisol production. Thus, a Catch-22 "degenerative cascade"
begins, which can be very difficult to stop.

Cortisol and
Brain Degeneration-Study

Studies done by
Dr. Robert M. Sapolsky, Professor of Neurology and Neurological Sciences at
Stanford University, showed that lots of stress or exposure to cortisol accelerates the degeneration of the
aging hippocampus.

And, because the hippocampus is part of the
feedback mechanism that signals when to stop cortisol production, a damaged
hippocampus causes cortisol levels to get out of control – further compromising
memory and cognitive function. The cycle of degeneration then
continues. (Perhaps similar to the deterioration of the pancreas-insulin
feedback system.

Cortisol Levels
During Human Aging-Study

The study was
titled "Cortisol levels during human aging predict hippocampal atrophy and
memory deficits". A third of the 60 volunteers, who were between ages 60
and 85, had chronically high cortisol levels, a problem that seems to be fairly
common in older people.13

The size of the
hippocampus averaged 14% smaller in one group and showed high and rising
cortisol levels, compared to a group with moderate and decreasing levels. The
small hippocampus group also did worse at remembering a path through a human
maze and pictures they'd seen 24 hours earlier and – two tasks that use the hippocampus.

Kindling and stress—how experience affects the brain:

Is it possible that chronic
stress, through a process called kindling, can create hard-wired,
hypersensitive neural networks capable of dictating and automating symptoms
from a wide range of instinctual behavior patterns? In his video course, Biology and Human Behavior: The
Neurological Origins of Individuality, 2nd edition, Robert M. Sapolsky examines how communication between neurons is strengthened
as a result of experience. When the dendritic spines of neurons are stimulated rapidly,
the synapses between the communicating neurons become "hyper-responsive or
potentiated" due to chemical changes within the neural environment.
Subsequently, less stimulation is necessary to again prod the neuron to
fire—the moment when an electrical signal bursts through the neuron's axon,
prompting release of chemical messengers called neurotransmitters into the
synapse between neurons, often increasing the likelihood that other neurons
will fire in a sort of chain reaction. In other words, Sapolsky says, the
neuron's "action potential" is increased. What's called
"long-term potentiation" is thus the basis for learning and memory,
possibly including injurious forms of learning such as post-traumatic stress
disorder (PTSD).

In Listening to Prozac: A
Psychiatrist Explores Antidepressant Drugs and the Remaking of the Self (1993), Peter D. Kramer writes, "Kindling rewires the brain. … the brain reshapes
itself anatomically in response to small noxious stimuli. … Kindling appears to
be a kind of learning, but a learning that can occur independent of cognition.
… Illness, once expressed, can become responsive to ever smaller stimuli and,
in time, independent of stimuli altogether. The expression of the disorder
becomes more complex over time."

In "Psychosomatic disease and the
'visceral' brain: Recent developments bearing on the Papez theory of emotion" (1949), Paul D. Maclean
theorized about the kindling process. "It is
possible that if a certain electrical pattern of information were to reverberate
for a prolonged period or at repeated intervals in the neuronal circuit, the
nerve cells (perhaps, say, as the result of enzymatic catalysis in the
dentritic processes at specific axone-dendritic junctions) would be permanently
'sensitized' to respond to this particular pattern at some future time. Such a
mechanism would provide for one variety of enduring memory in a way that is
remotely analogous to a wire recorder. These hypothetical considerations
suggest how oft-repeated childhood emotional patterns could persist to exert
themselves in adult life."

As MacLean suggests in using the term visceral, certain
reactions are not embedded in language and intellect, they are more like
"gut feelings" that can remain in primordial memory systems and that
can be strengthened through kindling. Winifred Gallagher explains kindling in
an article in The Atlantic Monthly, "How We Become What We Are" (September 1994).
Gallagher writes:

Over time, repeated stressful experiences can literally, not
just figuratively, alter the nervous systems of the temperamentally vulnerable.
Animal research has shown that when a rat is given a small shock, it shows no
marked reaction; when exposed to such stressors for five consecutive days, it
shows signs of the stress response; when exposed for seven or eight days, the
rat has a seizure, and thereafter this 'kindled' animal will seize with little
or no provocation.
Experiments of this kind are of course not done with people, but Philip Gold
and other neuroscientists now think that in human beings, too, by triggering a cascade
of chemical reactions, serious chronic stress, particularly in early life,
causes changes in the way genes within a brain cell function, permanently
altering the neuron's biology. Because they require a particular type of input
to turn on or off, only some of a neuron's thousands of genes, each of which is
involved in some aspect of cellular structure or communication, are activated
at any given moment. When a temperamentally vulnerable person is constantly bombarded with
upsetting stimuli, Gold says, the genes that get turned on are those involved
in the cellular components of the stress response."

I contend that neurotransmission in the amygdalae and their target
structures is sometimes kindled to generate dopamine-driven behaviors
aimed at solving problems including restoring order, control, and most
importantly–confidence. Under normal circumstances, this could be construed as
a survival instinct. Under extreme stress, however, especially when an outlet
for pent-up energy is not available, these behaviors may turn into obsessions
or compulsions. We will discuss such neurotransmission in greater detail in
Part 3 of MyBrainNotes.com. For now, I would like to point out that in Monkeyluv and Other Essays on Our
Lives as Animals (2005),
Robert M. Sapolsky describes how monkeys release dopamine in anticipation
of a food reward. They get most excited when a light first comes on signaling
that they may now perform a learned task and upon completion, will receive
food. Their excitement does not peak when the food finally appears; it peaks
well before that point. Sapolsky writes, "It's about the anticipation
of reward. It's about mastery and expectation and confidence."

...

Another example of kindling, which we discuss above, is the
effects of stress on the hippocampi. In his 1995 New York Times article
titled, "Severe Trauma May Damage the
Brain as Well as the Psyche," Daniel Goleman explains that studies in rats and primates
suggest that glucocorticoids are the culprit. Goleman quotes Robert Sapolsky,
who explains that glucocorticoids "may be neurotoxic to the hippocampus at
the massive levels that are released under extreme stress or during trauma. I'm
talking about the levels you would see in a zebra running from a lion, or a
person fleeing a mugger—a real physical life-and-death crisis—if it is repeated
again and again as time goes on."

If the glucocorticoids released during extreme stress and trauma
damage the hippocampi, it is no wonder that, according to Sapolsky in Why
Zebras Don't Get Ulcers, "there is atrophy of the hippocampus in long-term
depression. The atrophy emerges as a result of
the depression (rather than precedes it), and the longer the depressive
history, the more atrophy and the more memory problems."

Sapolsky points to the work of psychologists Martin Seligman and
Steven Maier who exposed animals to "pathological amounts" of stress.
"The result is a condition strikingly similar to a human depression."
Sapolsky explains that it is "repeated" stress that generates
depressive symptoms combined with "a complete absence of control on the
part of the animal." In other words, the animal has no outlets that can be
used to vent frustration. "When it
comes to what makes for psychological stress, a lack of predictability and
control are at the top of the list of things you want to avoid," Sapolsky
writes.

Sapolsky calls attention to the work of Joseph LeDoux of New York University,
"who pretty much put the amygdala on the map when it comes to
anxiety." In a way that only he can do, Sapolsky sums up the paradox
between severe, traumatic stress and its effect on the hippocampi versus the
amygdalae. "Suppose a major traumatic
stressor occurs, of a sufficient magnitude to disrupt hippocampal function
while enhancing amygdaloid function. At some later point, in a similar setting,
you have an anxious, autonomic state, agitated and fearful, and you haven't a
clue why—this is because you never consolidated memories of the event via your
hippocampus while your amygdala-mediated autonomic pathways sure as hell
remember."

We found that amygdala
volume correlates with the size and complexity of social networks in adult
humans. An exploratory analysis of subcortical structures did
not find strong evidence for similar relationships with any other structure,
but there were associations between social network variables and cortical
thickness in three cortical areas, two of them with amygdala connectivity.
These findings indicate that the amygdala is important in social behavior.

...

In this study
we examined whether amygdala volume varies with individual variation in the
size and complexity of social groupings within a single primate species,
humans. In 58 healthy adults (22 females; mean age M = 52.6, s.d. =
21.2, range = 19–83 years) with confirmed absence of DSM-IV Axis I diagnoses
and normal perform­ance on cognitive testing, we examined social network size
and com­plexity with two subscales of the Social Network Index (SNI9).

Linear regression
analyses revealed that individuals with larger and more complex social networks
had larger amygdala volumes (Fig. 1).

[5] Wikipedia, the free encyclopedia; Amygdala

Social interaction

Amygdala volume
correlates positively with both the size (the number of contacts a person has)
and the complexity (the number of different groups to which a person belongs)
of social networks.[41][42] Individuals with larger amygdalae had larger and more complex social
networks. They were also better able to make accurate social judgments about
other persons' faces.[43] It is hypothesized that larger amygdalae allow for greater emotional
intelligence, enabling greater societal integration and cooperation with
others.[44]